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BOD I > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

-itis

A

inflammation

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2
Q

-osis

A

degeneration

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3
Q

–oma, -trophy, -plasia

A

disorders of growth

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4
Q

-opathy

A

uncertain pathogenesis

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5
Q

what causes enlargement of cells

A

glycogen
hypertrophy of organelles
storage changes/error in metabolism (e.g. lysosomal storage disease

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6
Q

hyaline

A

homogenous, glossy appearance
describes IC proteins depositions (russel bodies, metal inclusions, viral inclusions)
describes EC protein deposits (edema fluid, fibrin, amyloid)

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7
Q

causes of amyloid

A

EC protein deposits composed of protein fibrils in beta pleated sheet

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8
Q

AA Amyloid

A

serum amyloid A

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9
Q

AL Amyloid

A

Ig light chains

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10
Q

AF Amyloid

A

prealbumin

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11
Q

endocrine amyloid

A

hormone and hormone-like proteins

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12
Q

type of amyloid in glomeruli in dogs, hepatic sinusoids in birds

A

AA amyloid

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13
Q

type of amyloid in lymphoid follicles

A

AL amyloid

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14
Q

type of amyloid in pancreatic islets or renal medulla in cats

A

endocrine amyloid

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15
Q

biochemical features of amyloid

A

insoluble
indigestable

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16
Q

morphological features of amyloid

A

amorphous
hyaline
extracellular
stains red/orange with congo red
stains green with Thioflavine T

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17
Q

Some parenchymal cells have a few small round, perfectly clear cytoplasmic spaces

A

reversible fatty change

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18
Q

All parenchymal cells contain a very large, perfectly clear, round cytoplasmic space

A

irreversible fatty degeneration

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19
Q

Some parenchymal cells have modest cytoplasmic swelling

A

reversible hydropic change

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20
Q

All parenchymal cells are markedly swollen

A

irreversible hydropic degeneration

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21
Q

pyknosis

A

shrinkage, clumping of nuclear chromatin

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22
Q

karyorrhexis

A

nuclear fragmentations

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23
Q

karyolysis

A

nuclear fading

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24
Q

Pro-Oxidants

A

xanthine oxidase
fenton & haber weiss reactions
superoxide anion, singlet oxygen
hydroxyl radical
nitric oxide
hydrogen peroxide

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25
anti-oxidants
superoxide dismutase & catalase glutathione peroxidase/reductase vitamins A,C,E transferrin, lactoferrin, ceruloplasmin
26
ATP depletion role in cell injury
affects membrane transport, protein synthesis, lipogenesis, phospholipid turner, and metabolism
27
Ca influx role in cell injury
activates enzymes (phospholipases, proteases, ATPases, endonucleases)
28
mitochondrial injury role in cell injury
mitochondrial permeability transition --> signal for apoptosis
29
membrane damage/increased permeability role in cell injury
ATP depletion, Ca activates phospholipases and direct damage by toxins/viral proteins/complement/perforins/chemical/physical agents
30
ROS role in cell injury
damage membranes, proteins and nucleic acids
31
dry gangrene causes
frostbite or intoxicants
32
wet gangrene causes
digested/liquified by environmental flora
33
two concurrent processes of necrosis
1. enzymatic digestion 2. protein denaturation
34
necrosis features
karyolysis adjacent tissue unaffected RBC intact inflammation passive, degradative tissue response membrane injury and organelle damage
35
causes of metastatic mineralization
hypervitamin D renal disease primary hyperparathyroidism hyperadrenocorticism paraneoplastic syndromes (PTHrP)
36
where is metastatic mineralization commonly found
gastric mucosa blood vessels lungs kidney
37
are thrombi dystrophic or metastic mineralization
dystrophic due to presence of platelets and fibrin
38
apoptosis features
pyknosis & karyorrhexis no inflammation active process no tissue response DNA damage, no organelle damage increased cytoplasmic eosinophilia forms apopotic bodies
39
what intiiates apoptosis
extrinsic pathway intrinsic pathway perforin/granzyme pathway
40
increased apoptosis results in...
neurodegenerative disorders exacerbation of damage in ischemic injury virus-induced lymphocyte depletion in acquired immunity deficiency syndromes
41
decreased apoptosis results in...
neoplasia autoimmune diseases
42
breakdown products of lipids, granular golden brown; usually microscopic
lipofuscin
43
dark, gross appearance, primarily in the lungs, urban environments, incidental
carbon
44
incidental pigmentation of tissues in pigmented animals; commonly affects pleura and meninges
melanin
45
postmortem production of hydrogen sulfide by bacteria with rxn with Fe in hemoglobin to form insoluble iron sulfide
pseudomelanosis
46
yellow pigment from wound, bruising
hematoidin
47
lighter brown granular pigment, represents accumulations of Fe & apoferritin
hemosiderin
48
greenish-brown pigment usually not granular, seen within hepatocytes/bile canaliculi/renal tubular epithelium; may be bright yellow and stain all tissues in hemolytic anemia (jaundice)
bilirubin
49
pinpoint hemorrhage, up to 1mm, capillary injury, petechiation
petechia
50
larger hemorrhage, up to a few cm, paintbrush appearance
ecchymosis
51
petechiae and ecchymoses on mucous membranes
purpura
52
focal hemorrhage which produced mass-like lesion
hematoma
53
causes of hemorrhage
local - trauma, hypoxia, degenerative conditions systemic - coagulopathies, metabolic,, neoplastic, or infectious diseases
54
consequences of hemmorhage
primary - shock, space occupying lesions with disastrous consequences in CNS/pericardial sac secondary - resorption of fluid, RBC lysis and phagocytosis, fibrinolysis, scarring
55
local edema causes
venous obstruction lymphatic obstruction inflammation or vascular injury
56
generalized edema causes
cardiac edema (increased hydrostatic pressure) renal failure (decreased plasma oncotic pressure) hepatic failure (decreased plasma oncotic pressure)
57
physioloical (eating, exercise) & pathological (inflammaltion/injury)
active hyperemia
58
pathological (heart failure, mechanical, gravity - recumbent animals)
passive hyperemia
59
acute passive hyperemia
sudden occlusion (torsion, strangulation) anoxia
60
chronic passive hyperemia
long standing interference, not complete ischemia (heart failure) hypoxia
61
best to worst fates of thrombi
fibrinolysis organization and recanalization propagation embolism
62
antemortem clots vs postmortem
antemortem - attached to endothelium, lesion postmortem - not attached to endothelium, incidental, no lesion
63
pale, dry, fibrin and platelets, firm thrombi
arterial thrombi
64
large, dark red, shiny, cranberry sauce-like thrombi with RBC
venous thrombi
65
a raised infarction is _______
acute
66
a depressed infarcation is _____
chronic
67
pale, light, anemic infarct is due to ____
arterial occlusion
68
dark, hemorrhagic infarct in tissues with dual circulation is due to _____
venous occlusion
69
how do you distinguish between an old infarct and new one
old has scar tissue, appears paler than adjacent tissue and smaller volume due to scarring
70
consequences of infarction
necrosis
71
which tissues are the most vulnerable to infarcts? least vulnerable?
most vulnerable - single perfusion organs - brain, heart, renal cortex least vulnerable - dual blood supply organs - liver & lungs - must occlude both bronchial a. and pulmonary a. for lungs and both hepatic a. and portal v. for liver
72
pro-coagulant factors for hemostasis
endothelial cells only: VWF collagen ADP and TXA2 tissue factor Ca2+ clotting factors platelet-activating factor plasminogen activator inhibitor (PAI) alpha2 antiplasmin
73
anti-coagulants factors for hemostasis
endothelial cells & blood proteins involved: covering thrombogenic subendothelial collagen NO and PGI2 Antithrombin III Thrombomodulin Plasminogen activators (t-PA and urokinase-like PA) antithrombins & protein C&S

BOD I (7 decks)

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